Modulation of cholinergic neurotransmission by the peptide VIP, VIP antiserum and VIP antagonists in dog and cat trachea.
Hakoda. H H; Ito. Y Y
Key Findings
- VIP at concentrations above 10⁻⁸ M hyperpolarizes airway smooth‑muscle cells and lowers their input resistance.
- VIP reduces the size of nerve‑evoked muscle contractions and the associated excitatory junction potentials (EJPs).
- VIP does not affect the muscle’s direct response to acetylcholine, and an antiserum against VIP has little impact on these effects.
- During repeated low‑frequency stimulation, VIP enhances the natural decline of EJPs, and during high‑frequency stimulation it dampens the buildup of EJPs.
Practical Outcomes
- For biohackers, this research shows that VIP can modulate airway nerve signaling in animals, but it offers no clear, actionable protocol for humans. The findings are more relevant to basic respiratory physiology than to longevity, metabolism, or performance optimization.
Summary
The study looked at how a peptide called VIP (and related blockers) affects nerve signals that make airway muscles contract in dogs and cats. It found that higher doses of VIP can calm these muscles by making the cells less excitable and reducing the strength of nerve‑driven contractions, but it doesn’t change how the muscles respond to acetylcholine directly.
Abstract
1. Comparative studies on the effects of vasoactive intestinal polypeptide (VIP), commercially available VIP antiserum or VIP antagonists [Ac-Tyr1, D-Phe2]-GRF(1-29)-NH2 and [4-Cl-D-Phe6, Leu17]-VIP on excitatory neuroeffector transmission in the dog and cat trachea were performed with microelectrode, double sucrose-gap, and tension recording methods. 2. VIP (10(-11)-10(-9) M) had no effect on the resting membrane potential or on the input resistance of the smooth muscle cells of dog and cat trachea. However, with increased concentrations (greater than 10(-8) M) VIP hyperpolarized the membrane and decreased the input resistance of the membrane in both tissues. 3. VIP (10(-10)-10(-7) M) dose-dependently reduced the amplitude of the contractions evoked through the nervous structure excited by field stimulation in the combined presence of indomethacin (10(-5) M) and guanethidine (10(-6) M) in the dog, and in the presence of guanethidine (10(-6) M) in cat trachea. In parallel with actions on twitch contractions, VIP (10(-11)-10(-7) M) reduced the amplitude of the excitatory junction potentials (EJPs) evoked through the nervous structure excited by single pulse field stimulation in both tissues. 4. VIP (10(-9) M) had no effect on the post-junctional response of smooth muscle cells to exogenous acetylcholine (ACh) (10(-9)-10(-5) M). 5. During repetitive field stimulation at the stimulus frequency of 0.033-0.1 Hz, the amplitude of the EJPs was gradually reduced, and VIP (10(-9) M) enhanced this depression phenomenon in the dog and cat trachea. 6. EJPs also showed summation when repetitive field stimulation was applied at high frequency (20 Hz) in the dog trachea. The slope of the relationship between the relative amplitude of the EJP and number of stimuli at 20 Hz was 2.2 +/- 0.4 mV/stimulation (n = 4) in the dog trachea. However, in the cat trachea, summation of EJPs was not prominent, giving a mean slope of 0.6 +/- 0.2 mV/stimulation (n = 6) measured by the microelectrode method. VIP (10(-9) M) shifted downward the relationship between the relative amplitude of the EJP and the number of stimuli at 20 Hz in both tissues. 7. Overnight incubation with VIP antiserum (10(-6) g/ml) had little effect on the depression of the EJP in the dog and cat trachea, or the summation of the EJP observed in the dog trachea.(ABSTRACT TRUNCATED AT 400 WORDS)
Study Information
pubmed
1990
1990-09-01T00:00:00.000Z
10.1113/jphysiol.1990.sp018204
33
37